OliPass Corporation, a South Korea based biotech specialized in the development of RNA therapeutics, announced that it is expanding its Scientific Advisory Board ("SAB") for SCN9A antisense pain killer OLP-1002 to include Professor Patrick M. Dougherty of The University of Texas MD Anderson Cancer Center and Professor Robert H. Dworkin of University of Rochester Medical Center. Professor Dougherty and Professor Dworkin will advise OliPass on Phase 2 clinical trials of OLP-1002.

"OLP-1002 is well-suited to management of neuropathic pain based on its mode of action. Considering the pharmacological complexity of neuropathic pain, however, expertise in neuropathic pain and in clinical study design will be critical to a success in the clinical development of OLP-1002 against neuropathic pain. We are very much honored to have Professor Dougherty and Professor Dworkin as new SAB members as we develop the first-in-class pain killer. Given that OLP-1002 is planned to be evaluated for a Phase 2a trial in patients with chemotherapy-induced peripheral neuropathy (CIPN), in-depth advice and guidance by these two high profile experts will add a critical element to the clinical validation of OLP-1002 against neuropathic pain", said Dr. Shin Chung, the founder and CEO of OliPass Corporation. "We are more than pleased that Profs. Dougherty and Dworkin are joining the OliPass SAB. With their addition, the OliPass SAB has unparalleled expertise. Added to OliPass' unique technology, in-house talent, and focus, this poises the company to move rapidly and effectively toward the much-needed goal of development of a new, effective, non-addictive therapy for chronic pain" noted SAB chairperson Prof. Stephen Waxman.

Prof. Dougherty has made multiple contributions toward a multidisciplinary understanding of the neurochemical and physiological consequences of peripheral injury and inflammation on neural activity in the CNS. He has significantly contributed to defining mechanism of cancer therapy-induced pain and identifying potential therapeutic interventions for its relief or prevention. Prof. Dworkin has unique expertise on methodologic aspects of pain clinical trials. He has served as consultant to and member of multiple US FDA and CDC advisory/working groups, and led a large number of clinical trials of pain medications as principal investigator.

The two experts will join the OliPass SAB chaired by Prof. Waxman who led a team that identified sodium ion channel Nav1.7, the product of gene SCN9A, as a key regulator of pain. He has since contributed to studies that have provided evidence that Nav1.7 blockers can reduce pain in erythromelalgia (man-on-fire syndrome) and trigeminal neuralgia. He served as chairman of neurology at Yale University, and he founded and directs the Neuroscience & Regeneration Research Center at Yale.

About SCN9A Pain Killer OLP-1002

OLP-1002 is an extremely potent antisense OPNA (OliPass Peptide Nucleic Acid) selectively targeting the SCN9A pre-mRNA to induce exon skipping, and selectively inhibit the expression of Nav1.7. OLP-1002 is expected to reproduce much of the clinical phenotype of people with a loss-of-function mutation in the SCN9A gene. Unlike small molecule Nav1.7 inhibitors with limited Nav1.7 selectivity, OLP-1002 may safely treat various types of pain as a selective inhibitor of Nav1.7. Considering that there are not many safe therapeutic options available for chronic pain, neuropathic pain, cancer pain and various types of refractory pain, OLP-1002 shall replace currently prevailing pain killers such as NSAIDs, opioids, anti-depressants, and anti-epileptic drugs. The strong efficacy and excellent safety of OLP-1002 shall change our views of pain killers and trigger rapid growth of the global pain killer market of currently stagnant at 100 billion USD per year.

About Clinical Outcomes with OLP-1002

OLP-1002 was found safe and well-tolerated in a Phase 1 trial evaluated in a total of 116 healthy volunteers in UK. There were no suggestions of QT elongation at all tested doses of OLP-1002 (30 ng to 160 mcg), demonstrating excellent Nav1.7 selectivity over the other subtypes of sodium ion channel. In a Phase 1b trial evaluated in a relatively small number of osteoarthritis (OA) patients in Australia, OLP-1002 was also found safe and showed a strong trend of pain relief as the dose was increased from 5 mcg to 10 mcg. OLP-1002 shall be soon subjected to a Phase 2a study in a larger number of OA patients to titrate therapeutic doses meeting the target efficacy and therapeutic duration. "OA pain is readily manageable by knocking down Nav1.7 either in PNS (peripheral neuronal system) or in CNS (central neuronal system) by selecting clinical dose. It will be interesting to compare the clinical outcomes of Nav1.7 knockdown in PNS only with those in CNS. In this regard, OA pain may serve as a good clinical model to assess either peripheral or central contribution of Nav1.7 for other types of pain", commented Dr. Chung on OA pain trials. OliPass is planning Phase 2 proof of principle studies of OLP-1002 in chemotherapy induced peripheral neuropathy (CIPN). At least half of patients receiving chemotherapy or immunologic cancer therapy develop numbness, tingling or sensory motor impairment. About half of them will develop pain and in some cases severe enough to detract substantially from quality of life and to limit the dosage of cancer therapy that a patient can tolerate. Existing pain therapies are not effective.  Thus CIPN represents a high unmet medical need.

About OliPass Corporation

OliPass Corporation is a publically traded biotech company listed in KOSDAQ in South Korea (ticker: KQ244460). The company is developing RNA therapeutics based on its proprietary oligonucleotide platform called OPNA (OliPass Peptide Nucleic Acid). OPNA was derived from PNA by rational chemical modifications in order to improve the cell permeability and RNA affinity. For therapeutic intervention, OPNA potently binds to target pre-mRNA, induces exon skipping, and yields mRNA splice variant. Unlike other types of RNA therapeutics, OPNA does not require formulation aid for in vivo therapeutic activity.